沂沭断裂带构造地貌格局及其形成与演化

沂沭断裂带表现为东西分带、南北分段的棋盘格式构造地貌格局.这种构造地貌格局是由于受到北北东一南南西向挤压作用,断裂带两端受到近南一北向挤压作用而形成的;其形成及发展经历了四个主要阶段.     

真应力应变曲线的自动测试

介绍材料力学实验中的微机自动测试系统及其测试:真应力应变全程曲线和屈服极限σ_s,强度极限σ_b、延伸率δ、颈缩率ψ的自动测试方法。并结合实例说明了软件和横向位移传感器的结构设计。     

钢制压力容器筒体中的残余应力

应用弹塑性理论分析了钢制压力容器简体在制造成型时产生的残余应力，指出按中径公式设计时不应忽视残余应力，建议将简体由四周向水压试验应力控制在０．８［σ］之内．     

水分胁迫对小麦叶片内源多胺的累积和乙烯产生的影响

用春小麦陇春１０号Ｌｏｎｇｃｈｕｅｎ ｎｏ．１０各旱选４号Ｈａｎｘｕａｎ Ｎｏ．４的幼苗为材料研究了－１．０Ｍｐａ ＰＥＧ溶液胁迫处理对叶内多胺含量和乙烯产生的影响及品种间的差异。     

Bacterial suicide through stress

Outside of the laboratory, bacterial cells are constantly exposed to stressful conditions, and an ability to resist those stresses is essential to their survival. However, the degree of stress required to bring about cell death varies with growth phase, amongst other parameters. Exponential phase cells are significantly more sensitive to stress than stationary phase ones, and a novel hypothesis has recently been advanced to explain this difference in sensitivity, the suicide response. Essentially, the suicide response predicts that rapidly growing and respiring bacterial cells will suffer growth arrest when subjected to relatively mild stresses, but their metabolism will continue: a burst of free-radical production results from this uncoupling of growth from metabolism, and it is this free-radical burst that is lethal to the cells, rather than the stress per se. The suicide response hypothesis unifies a variety of previously unrelated empirical observations, for instance induction of superoxide dismutase by heat shock, alkyl-hydroperoxide reductase by osmotic shock and catalase by ethanol shock. The suicide response also has major implications for current [food] processing methods. Received 29 March 1999; received after revision 14 May 1999; accepted 17 May 1999     

Oxidative stress and hypoxia-like injury cause Alzheimer-type molecular abnormalities in central nervous system neurons

Neuronal loss and neuritic/cytoskeletal lesions (synaptic disconnection and proliferation of dystrophic neurites) represent major dementia-associated abnormalities in Alzheimer’s disease (AD). This study examined the role of oxidative stress as a factor contributing to both the cell death and neuritic degeneration cascades in AD. Primary neuron cultures were treated with H₂O₂ (9–90 μM) or desferrioxamine (2–25 μM) for 24 h and then analyzed for viability, mitochondrial mass, mitochondrial function, and pro-apoptosis and sprouting gene expression. H₂O₂ treatment causes free-radical injury and desferrioxamine causes hypoxia-type injury without free radical generation. The H₂O₂-treated cells exhibited sustained viability but neurite retraction, impaired mitochondrial function, increased levels of the pro-apoptosis gene product CD95/Fas, reduced expression of N2J1-immunoreactive neuronal thread protein and synaptophysin, and reduced distribution of mitochondria in neuritic processes. Desferrioxamine treatment resulted in dose-dependent neuronal loss associated with impaired mitochondrial function, proliferation of neurites, and reduced expression of GAP-43, which has a role in path-finding during neurite outgrowth. The results suggest that oxidative stress can cause neurodegeneration associated with enhanced susceptibility to apoptosis due to activation of pro-apoptosis genes, neurite retraction (synaptic disconnection), and impaired transport of mitochondria to cell processes where they are likely required for synaptic function. In contrast, hypoxia-type injury causes neuronal loss with proliferation of neurites (sprouting), impaired mitochondrial function, and reduced expression of molecules required to form and maintain synaptic connections. Since similar abnormalities occur in AD, both oxidative stress and hypoxic injury can contribute to AD neurodegeneration. Received 24 May 2000; received after revision 7 July 2000; accepted 27 July 2000     

电阻应变测量技术在压力容器检验中的应用

介绍了电阻应变测量技术的测试原理和测试方法，并结合化工企业对压力容器检验的技术要求，应用电阻应变测量技术对典型压力容器作出了应力分析和安全评定。     

甲基丙烯酸镁补强丁腈橡胶的拉伸应力-应变行为

研究了单轴拉伸时甲基丙烯酸镁补强丁腈橡胶的应力 -应变行为 .采用 Gregory提出的储能函数形式 ,描述了甲基丙烯酸镁补强丁腈橡胶的应力 -应变行为 .结果表明 ,根据该形式所得的理论曲线在整个实验所及的应变范围内均能与实验曲线很好地符合 .另外 ,还研究了甲基丙烯酸镁补强丁腈橡胶的应力松弛及应力软化现象     

Ti/Cu/不锈钢爆炸复合界面层的电子显微组织

采用扫描电镜(SEM)与电子探针(EPMA)研究了Ti(合金)/Cu/不锈钢(S.S)爆炸复合界面层的电子显微组织特征,分析了界面层成分再分布规律及化合物的形成。结果表明,CU/S.S界面层具有明显的爆炸焊接波状组织,波长约200μm。Ti/Cu界面层呈锯齿波状,比较细小,波长仅30～40μm。在中间过渡层Cu,观察到大量的应力应变流线,显示爆炸复合过程冲击波流动特征。SEM照片及EPMA合析结果表明:在高温、高压、快速爆炸焊接过程中存在着复杂的冶金物理反应,形成多种反应产物。界面层除发生塑性形变外,还存在相互扩散,熔化和回复再结晶。     

4-Hydroxynonenal-modified amyloid-beta peptide inhibits the proteasome: possible importance in Alzheimer's disease

The amyloid β-peptide (Aβ) is a 4-kDa species derived from the amyloid precursor protein, which accumulates in the brains of patients with Alzheimer’s disease. Although we lack full understanding of the etiology and pathogenesis of selective neuron death, considerable data do imply roles for both the toxic Aβ and increased oxidative stress. Another significant observation is the accumulation of abnormal, ubiquitin-conjugated proteins in affected neurons, suggesting dysfunction of the proteasome proteolytic system in these cells. Recent reports have indicated that Aβ can bind and inhibit the proteasome, the major cytoslic protease for degrading damaged and ubiquitin-conjugated proteins. Earlier results from our laboratory showed that moderately oxidized proteins are preferentially recognized and degraded by the proteasome; however, severely oxidized proteins cannot be easily degraded and, instead, inhibit the proteasome. We hypothesized that oxidatively modified Aβ might have a stronger (or weaker) inhibitory effect on the proteasome than does native Aβ. We therefore also investigated the proteasome inhibitory action of Aβ _1–40 (a peptide comprising the first 40 residues of Aβ) modified by the intracellular oxidant hydrogen peroxide, and by the lipid peroxidation product 4-hydroxynonenal (HNE). H₂O₂ modification of Aβ _1–40 generates a progressively poorer inhibitor of the purified human 20S proteasome. In contrast, HNE modification of Aβ _1–40 generates a progressively more selective and efficient inhibitor of the degradation of fluorogenic peptides and oxidized protein substrates by human 20S proteasome. This interaction may contribute to certain pathological manifestations of Alzheimer’s disease Received 26 September 2000; accepted 26 September 2000